ArticleBritish journal of cancer2020
Suppression of G6PD induces the expression and bisecting GlcNAc-branched N-glycosylation of E-Cadherin to block epithelial-mesenchymal transition and lymphatic metastasis.
Article in British journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- G6PD: An Old Player with Multiple Emerging Roles from Cancer Progression to Metastasis and Chemoresistance.The protein journal · 2026Review
- CircNOLC1/KRT16 promotes colorectal cancer invasion and migration via c-met nuclear translocation and reprogramming of the oxidative pentose phosphate pathway.The Journal of biological chemistry · 2026Article
- NADPH-Related Enzymes and Cancer: Facts and Insights Into the Application of Immunohistochemistry.Biochemistry research international · 2026Review
- Deciphering context-specific Axitinib escape pathways via multi-omics and explainable machine learning.Journal of translational medicine · 2025Article
- Exploring Metabolic and Immunological Biomarkers for Oral Squamous Cell Carcinoma: Potential Targets for Precision Therapy.Biology · 2025Review
- Somatic CRISPR tumorigenesis and multiomic analysis reveal a pentose phosphate pathway disruption vulnerability in MPNSTs.Science advances · 2025Article
- Downregulation of MGAT3 Promotes Benzo[ACS omega · 2025Article
- Metformin upregulates circadian gene PER2 to inhibit growth and enhance the sensitivity of glioblastoma cell lines to radiotherapy via SIRT2/G6PD pathway.Frontiers in pharmacology · 2025Article
- The Role of Glucose-6-Phosphate Dehydrogenase in Skin Cancer Metabolism: A Paradigm Shift in Treatment Approaches.Cancers · 2024Review
- Connecting the dots: investigating the link between environmental, genetic, and epigenetic influences in metabolomic alterations in oral squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2024Review
- Metabolic Signaling in Cancer Metastasis.Cancer discovery · 2024Review
- Identification of AURKA as a Biomarker Associated with Cuproptosis and Ferroptosis in HNSCC.International journal of molecular sciences · 2024Article
- Bisecting GlcNAc modification reverses the chemoresistance via attenuating the function of P-gp.Theranostics · 2024Article
- IL-6/JAK2-dependent G6PD phosphorylation promotes nucleotide synthesis and supports tumor growth.Molecular metabolism · 2023Article
- Fibromodulin overexpression drives oral squamous cell carcinoma via activating downstream EGFR signaling.iScience · 2023Article
- Zinc Finger Proteins in the War on Gastric Cancer: Molecular Mechanism and Clinical Potential.Cells · 2023Review
- Inhibitory Effect of Phosphorothioate Oligonucleotide Complementary to G6PD mRNA on Murine Melanoma.Current issues in molecular biology · 2023Article
- The role of N-glycosylation modification in the pathogenesis of liver cancer.Cell death & disease · 2023Review
- Article
- Downregulated HDAC3 or up-regulated microRNA-296-5p alleviates diabetic retinopathy in a mouse model.Regenerative therapy · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundAs the rate-limit enzyme of the pentose phosphate pathway, glucose-6-phosphate dehydrogenase (G6PD) plays important roles in tumour progression, but the exact mechanism through which G6PD controls cancer metastasis remains unclear.
methodsG6PD expression in resected oral squamous cell carcinoma (OSCC) samples was analysed by immunohistochemistry. The effects and mechanism of G6PD suppression on OSCC cell lines were measured by transwell assay, wound healing assay, western and lectin blot, mass spectrometer analysis, ChIP-PCR, and luciferase reporter assay. BALB/c-nude mice were used to establish orthotopic xenograft model.
resultsG6PD expression in the tumours of 105 OSCC patients was associated with lymphatic metastasis and prognosis. In vitro cellular study suggested that G6PD suppression impaired cell migration, invasion, and epithelial-mesenchymal transition. Furtherly, G6PD knockdown activated the JNK pathway, which then blocked the AKT/GSK-3β/Snail axis to induce E-Cadherin expression and transcriptionally regulated MGAT3 expression to promote bisecting GlcNAc-branched N-glycosylation of E-Cadherin. An orthotopic xenograft model further confirmed that dehydroepiandrosterone reduced lymphatic metastatic rate of OSCC, which was partially reversed by JNK inhibition.
conclusionsSuppression of G6PD promoted the expression and bisecting GlcNAc-branched N-glycosylation of E-Cadherin via activating the JNK pathway, which thus acted on OSCC metastasis.
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